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ARS Home » Midwest Area » Peoria, Illinois » National Center for Agricultural Utilization Research » Crop Bioprotection Research » Research » Publications at this Location » Publication #158106


item Gorsich, Steven
item SHAW, J

Submitted to: Molecular Biology of the Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/6/2004
Publication Date: 10/1/2004
Citation: Gorsich, S.W., Shaw, J.M. 2004. The role of mitochondrial fission and fusion during meiosis and sporulation in yeast. Molecular Biology of the Cell. 15(10):4369-4381.

Interpretive Summary: In times of environmental stress, yeast/fungi will form protective spores that will germinate when environmental conditions improve. Mitochondria are essential cellular structures that are responsible for generating most of the cell's energy through respiration. Thus, the ability of yeast spores to inherit mitochondria is essential for spore survival and respiratory fitness upon germination. For successful industrial application, improved spore survival and fitness are desired. In this study, using various yeast mutants with known mitochondrial morphology defects, we showed that by altering mitochondrial morphology, yeast spores inherit mitochondria poorly which directly compromises their survival and respiratory function. These results suggest that targeted mitochondrial mutation methods could be used in the future to increase fitness of industrially important yeast/fungi, or potentially, to eliminate pathogens.

Technical Abstract: The network of tubular mitochondria in yeast is maintained by opposing fission and fusion events. At least six proteins regulate these membrane dynamics during mitotic growth. Dnm1p, Mdv1p and Fis1p are required for fission. Fzo1p, Mgm1p, and Ugo1p are required for fusion. Previous studies established that mitochondrial compartments fragment and rejoin at distinct stages during meiosis and sporulation, raising the possibility that mitochondrial fission and fusion events are required during this process. Here we report that strains defective for mitochondrial fission alone, or both fission and fusion, complete meiosis and sporulation. However, visualization of GFP-labeled mitochondria in sporulating cultures reveals morphological defects associated with the loss of fusion and/or fission proteins. Specifically, mitochondria collapse to one side of the cell and fail to fragment during pre-sporulation. In addition, mitochondrial compartments are not inherited equally by newly formed spores, resulting in decreased spore viability. Labeling studies reveal additional mitochondrial DNA nucleoid distribution and segregation defects that give rise to spores lacking detectable nucleoids. This nucleoid inheritance defect is correlated with an increase in respiratory incompetent spore colonies. Unexpectedly, when fission proteins are absent during sporulation, mitochondria still fragment in mature tetrads. The latter finding suggests that: 1) a novel mitochondrial fission machinery operates during yeast sporulation, or 2) mechanical forces generate the mitochondrial fragments observed in mature spores. These combined results provide evidence of fitness defects caused by mitochondrial fission mutations and reveal new phenotypes associated with mitochondrial fission and fusion mutations.